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Editorial
February 2016

Oral Cancer Chemoprevention—The End of EPOC, the Beginning of an Epoch of Molecular Selection

Author Affiliations
  • 1Division of Hematology/Oncology, Department of Internal Medicine, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania
  • 2Department of Otolaryngology, University of California San Francisco, San Francisco
JAMA Oncol. 2016;2(2):178-179. doi:10.1001/jamaoncol.2015.4637

The promise of chemoprevention of head and neck squamous cell carcinoma (HNSCC) was first raised in 1953 in an article by Slaughter et al1 describing epithelial field cancerization, or premalignant changes within grossly normal mucosa adjacent to invasive oral cancers. Slaughter et al hypothesized that an “as-yet-unknown” carcinogen condemned the entire oral mucosa toward malignant progression. Environmental carcinogens, including tobacco and alcohol, are now recognized causes of epithelial field cancerization. Patients curatively treated for a first human papillomavirus-negative HNSCC demonstrate the highest rate of second primary tumor (SPT) formation among patients with cancer. This major source of morbidity and mortality has motivated 3 decades of research in HNSCC chemoprevention. However, no effective and well-tolerated agent has been identified. In this issue of JAMA Oncology, William and colleagues2 present results from the EPOC (Erlotinib Prevention of Oral Cancer) study, a randomized chemoprevention trial evaluating whether the small molecule epidermal growth factor receptor (EGFR) inhibitor erlotinib prevents HNSCC in patients with high-risk oral premalignant lesions (OPLs). Despite compelling rationale, the EPOC study demonstrated that 12 months of erlotinib failed to improve oral cancer-free survival (CFS) vs placebo.

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